Cellularity and apoptosis after radiofrequency-induced shrinkage of collagenous tissue
DOI:
https://doi.org/10.1080/17453670510041466Abstract
Background Electrothermally-assisted capsular shrinkage has been gaining increased acceptance in the treatment of shoulder instability. Its indication in ACL-deficient knees has been discussed recently. Methods We examined the influence of immobilization on cell homeostasis of healing collagenous tissue after radiofrequency energy was applied to the patellar tendon in 23 rabbits. The animals were killed immediately after surgery (n = 6) or 3 weeks after surgery (n = 17). 10 rabbits were allowed normal cage activity, whereas the treated hind limb of 7 animals was immobilized for 3 weeks in a cast. Feulgen staining was used to stain the DNA of cell nuclei. Cells undergoing apoptosis were identified by the TUNEL method. Quantitative histological assessment was performed using imaging analysis software. Results Severe cellular damage in RF-treated collagenous tissue was partly induced by the immediate onset of apoptosis. At 3 weeks after surgery, non-immobilized tendon showed increased cellularity and apoptosis, whereas immobilization prevented the increase in cellularity and apoptosis significantly. The calculated ratio of apoptosis was not influenced by any postoperative treatment. Interpretation Diminished cellularity and apoptosis during tissue remodeling, due to immobilization, may protect the shortened collagenous scaffold from stretching and further optimize the clinical outcome after radiofrequency shrinkage. To stabilize the shrunken tissue, proliferation during postoperative wound healing should be minimized by careful rehabilitation.Downloads
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Published
2005-01-01
How to Cite
Kümpers, P., Pötzl, W., Heusner, T., Steinbeck, J., & Szuwart, T. (2005). Cellularity and apoptosis after radiofrequency-induced shrinkage of collagenous tissue. Acta Orthopaedica, 76(4), 487–495. https://doi.org/10.1080/17453670510041466
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Acta Orthopaedica (Scandinavica) content is available freely online as from volume 1, 1930. The journal owner owns the copyright for all material published until volume 80, 2009. As of June 2009, the journal has however been published fully Open Access, meaning the authors retain copyright to their work. As of June 2009, articles have been published under CC-BY-NC or CC-BY licenses, unless otherwise specified.
